06083nam 22017653a 450 991036756490332120250203235431.09783039213900303921390310.3390/books978-3-03921-390-0(CKB)4100000010106097(oapen)https://directory.doabooks.org/handle/20.500.12854/45331(ScCtBLL)82311094-2539-402e-b698-fb2d0c937a85(OCoLC)1163843152(oapen)doab45331(EXLCZ)99410000001010609720250203i20192019 uu engurmn|---annantxtrdacontentcrdamediacrrdacarrierDNA Replication StressRobert M. BroshMDPI - Multidisciplinary Digital Publishing Institute2019Basel, Switzerland :MDPI,2019.1 electronic resource (368 p.)9783039213894 303921389X This Special Issue of International Journal of Molecular Sciences (IJMS) is dedicated to the mechanisms mediated at the molecular and cellular levels in response to adverse genomic perturbations and DNA replication stress. The relevant proteins and processes play paramount roles in nucleic acid transactions to maintain genomic stability and cellular homeostasis. A total of 18 articles are presented which encompass a broad range of highly relevant topics in genome biology. These include replication fork dynamics, DNA repair processes, DNA damage signaling and cell cycle control, cancer biology, epigenetics, cellular senescence, neurodegeneration, and aging. As Guest Editor for this IJMS Special Issue, I am very pleased to offer this collection of riveting articles centered on the theme of DNA replication stress. The blend of articles builds upon a theme that DNA damage has profound consequences for genomic stability and cellular homeostasis that affect tissue function, disease, cancer, and aging at multiple levels and through unique mechanisms. I thank the authors for their excellent contributions, which provide new insight into this fascinating and highly relevant area of genome biology.Biology, life sciencesbicsscWerner SyndromeA549 cellsepigeneticneurodegenerationGenome integrityadaptationcellular senescencegenome instabilityWerner Syndrome Proteinlipofuscincell cycle checkpointsexonuclease 1template-switchingenergy metabolismmutation frequencyDNA replicationfork regressionmotor neuron diseaseMicrosatellitesAlzheimer's diseasechromatin remodelerrepair of DNA damageAP site analoguemutagensreplication timingThermococcus eurythermalisnucleolar stressgene expressionmutations spectraorigin firingFanconi Anemiasuperfamily 2 ATPaseDNA translocationDNA repairSSB signalinghomologous recombinationcommon fragile sites8-chloro-adenosinereplicationgenome stabilitymutagenicityfork reversalmultiple sclerosisnon-B DNAprotein stabilityheterogeneityubiquitinSenTraGorTM (GL13)replication restartEdU?-arrestinNERagingSSB end resectionoxidative stressATRdormant originsR loopsDNA damage responseDifficult-to-Replicate SequencesDNA double-strand repairendonuclease IVALSdouble strand break repairpremature agingreplication stressEXO1POL?translesion synthesisstrand displacementsG2-arrestDNA replication patternSSB repairgenome integrityG protein-coupled receptor kinase interacting protein 2 (GIT2)MMRreplicative stresssenolyticsspacerinteractomeATR-Chk1 DDR pathwayC9orf72replication fork restarttranslesion DNA synthesisDNA damagemismatch repairDNA replication stressDNA helicasePolymerase kappaDNA fiber assayH1299 cellsTLSAPE2ageingcell deathchromosomeTopBP1barleyclock proteinspost-translational modification8-oxoGS phaseataxia telangiectasia mutated (ATM)G protein-coupled receptor (GPCR)Polymerase etacancerG protein-coupled receptor kinase (GRK)helicasegenomic instabilityParkinson's diseasenucleotide excision repairSupFBiology, life sciencesBrosh Robert M1786458ScCtBLLScCtBLLBOOK9910367564903321DNA Replication Stress4318145UNINA